Free radicals mediate postshock contractile impairment in cardiomyocytes
Journal
Critical Care Medicine
Journal Volume
36
Journal Issue
12
Pages
3213-3219
Date Issued
2008
Author(s)
Abstract
OBJECTIVE: Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock. DESIGN: Randomized prospective animal study. SETTING: University affiliated research laboratory. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups. MEASUREMENTS AND MAIN RESULTS: DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% ± 2.5% to 5.6% ± 3.4% (p = 0.000) and the Ca transient decreased from 1.15 ± 0.13 au to 1.08 ± 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca transient. CONCLUSION: Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals. ? 2008 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.
SDGs
Other Subjects
ascorbic acid; calcium; free radical; fura 2; antioxidant; ascorbic acid; calcium; free radical; animal experiment; animal model; animal tissue; article; calcium transport; cell isolation; controlled study; drug effect; drug mechanism; electric shock; experimental animal; heart muscle cell; heart muscle injury; male; muscle contraction; muscle fiber contraction; nonhuman; priority journal; prospective study; rat; Sprague Dawley rat; animal; cardioversion; heart contraction; human; in vitro study; metabolism; physiology; randomization; Animals; Antioxidants; Ascorbic Acid; Calcium; Electric Countershock; Electroshock; Free Radicals; Humans; Male; Myocardial Contraction; Myocytes, Cardiac; Random Allocation; Rats; Rats, Sprague-Dawley
Type
journal article